Interactions between airway smooth murle cells and inflammatory cells in the pathogenesis of asthma
Interactions between airway smooth murle cells and inflammatory cells in the pathogenesis of asthma
批准号:
17390242
负责人:
TAKIZAWA Hajime
金额:
$10.5万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (B)
财政年份:
2005
资助国家:
日本
项目状态:
已结题
起止时间:
2005 至 2007
中文摘要
已有研究表明,气道平滑肌细胞在哮喘发病机制中具有重要作用,但其与T细胞、肥大细胞、嗜酸性粒细胞等炎性细胞之间的相互作用机制尚不清楚。IL-9是一类Th2型细胞因子,是作用于气道平滑肌细胞的强有力的诱导剂。呼吸道结构细胞曾被认为是终末分化细胞,但最近的报道强烈表明,即使是这些细胞也可能转化为其他类型的细胞。我们证明了人上皮细胞在转化生长因子β刺激下表现出明显的上皮间质转化(EMT)。这些变化是由肿瘤坏死因子α诱导的。提示呼吸道结构细胞与炎症细胞之间通过细胞因子和生长因子的动态相互作用在哮喘发病机制中的气道重塑调节中起重要作用。这些新发现可能突出了一种开发新型抗哮喘药物的途径,该药物可防止不可逆的呼吸道改变--重塑
英文摘要
It has been suggested that airway smooth muscle cells play important roles in the pathogenesis of asthma, but precise mechanisms remain unclear W efocused on the interactions between these structural cells and inflammatory cells such as T cells, mast cells and eosinophils Human airway smooth muscle cells express and release stem cell factor, TGF beat family molecules and and versican. These factors are believed to be chemotactic for mast cells and also be involved in airway wall remodling.IL-9, a class of Th2 type cytokine, is a potent inducer acting on airway smooth muscle cells.Airway structural cells are once believed to be terminally differentiated cells, but recent reports strongly suggest that even these cells may change in to other type of cells. We demonstrated that human epithelial cells showed a distinct epithelial mesenchymal transition (EMT) upon stimulation of TGFbeta. These changes were induced by TNFalpha. It was suggested that dynamic interactions between airway structural cells and inflammatory cells via cytokines and growth factors play important roles in the regulation of airway remodeling in the pathogenesis of asthma. These new finding may highlight a way to develop novel type of anti-asthma drugs preventing remodeling, an irreversible airway change
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Methotrexate induces proinflammatory cytokines production by human bronchial and alveolar epithelial cells
甲氨蝶呤诱导人支气管和肺泡上皮细胞产生促炎细胞因子
DOI:
--
发表时间:
2006
期刊:
影响因子:
--
作者:
[Yamauchi Y, et. al.]
通讯作者:
et. al.
DOI:
10.1080/01902140701884406
发表时间:
2008-03-01
期刊:
EXPERIMENTAL LUNG RESEARCH
影响因子:
1.7
作者:
[Li, Ying-Ji, Kawada, Tomoyuki, Kohyama, Tadashi]
通讯作者:
Kohyama, Tadashi
TGF-beta1 and serum both stimulate contraction but differentially affect apoptosis in 3D collagen gels.
TGF-β1 和血清均刺激收缩,但对 3D 胶原凝胶中的细胞凋亡影响不同。
DOI:
--
发表时间:
2006
期刊:
Respir Res 2;6:
影响因子:
--
作者:
[Matsumoto, A., Hiramatsu, K., Li, Y., Azuma, A., Kudoh, S., Takizawa, H., Sugawara, I, Kobayashi T et al., Fang Q et al., 幸山 正, Kobayashi T et al.]
通讯作者:
Kobayashi T et al.
DOI:
10.1016/j.clim.2006.08.003
发表时间:
2006-11-01
期刊:
CLINICAL IMMUNOLOGY
影响因子:
8.6
作者:
[Matsumoto, Aki, Hiramatsu, Kumiko, Sugawara, Isamu]
通讯作者:
Sugawara, Isamu
DOI:
10.1007/s40629-016-0093-5
发表时间:
2016
期刊:
Allergo journal international
影响因子:
--
作者:
[Lommatzsch M, Stoll P]
通讯作者:
Stoll P
共 22 条
Interactions of myofibroblasts with airway epithelial cells in allergic airway inflammation
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批准号:14570543
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项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$2.24万
-
财政年份:2002
-
负责人:TAKIZAWA Hajime
-
依托单位:
Molecular mechanisms of chemokine gene expression in allergic airway inflammation : Selective induction of eotaxin and TARC by Th2 cytokines in airway epithelial cells
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批准号:12670551
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.18万
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财政年份:2000
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负责人:TAKIZAWA Hajime
-
依托单位:
Role of airway epithelial cells in the accumulation and activation of T cells in allergic airway inflammation
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批准号:10670533
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.05万
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财政年份:1998
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负责人:TAKIZAWA Hajime
-
依托单位:
気管支喘息の気道傷害後の修復とリモデリングにおける成長因子の役割-特にトランスフォーミング成長因子β(TGFβ)を中心に-
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批准号:08670656
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项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$1.47万
-
财政年份:1996
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负责人:TAKIZAWA Hajime
-
依托单位:
海外基金